Highlights
- •A Mediterranean-style diet was inversely associated with left ventricular (LV) mass.
- •The association between a Mediterranean-style diet and LV mass may be partly mediated by obesity.
- •Consumption of cereals and grains and moderate alcohol use were associated with reduced LV mass.
One mechanism linking diet, specifically the Mediterranean-style diet (DT), with cardiovascular
disease prevention may be an association between a DT and left ventricular (LV) mass.
However, there are little data on this relation. We hypothesized that adherence to
a DT would be inversely associated with LV mass in the multiethnic population–based
Northern Manhattan Study. The study included 1,937 participants with diet assessments
and LV mass measured using echocardiography (mean age 67 ± 9 years, 39% male, 58%
Hispanic, 20% white, 20% black). A DT adherence score (range 0 to 9, 9 representing
maximal adherence) was examined continuously and categorically (score 6 to 9 representing
the top quartile vs 0 to 5). Multivariable-adjusted linear regression models were
constructed to examine the cross-sectional association between a DT and LV mass. An
inverse association was observed between the DT score and LV mass. In a model controlling
for demographics, behavioral risk factors, diabetes, and blood pressure variables,
LV mass was 1.98 g lesser for each 1-point greater DT score, and those with scores
of 6 to 9 had an average LV mass that was 7.30 g less than those with scores of 0
to 5. The association was attenuated but remained statistically significant after
additionally adjusting for body mass index. Results were similar when LV mass was
corrected for height (LV mass). In conclusion, greater adherence to a DT is associated
with decreased LV mass, an important risk factor for cardiovascular disease, and this
association may be partly mediated by obesity. The association with LV mass may be
involved in the protective effect of a DT on clinical vascular outcomes.
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Article info
Publication history
Published online: November 29, 2014
Accepted:
November 25,
2014
Received in revised form:
November 25,
2014
Received:
September 22,
2014
Footnotes
This work is supported by Grants R37 NS 29993 and R01 NS36286 from the National Institute of Neurological Disorders and Stroke, Bethesda, MD.
See page 514 for disclosure information.
Identification
Copyright
© 2015 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
